ArticleInternational journal of molecular sciences2022
Functional Expression of Choline Transporters in Microglia and Their Regulation of Microglial M1/M2 Polarization.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Olfml3 Regulates Microglial Inflammation and Neuronal Injury in Obstructive Sleep Apnea via Cybb-Mediated TLR4/NF-κB Pathway.CNS neuroscience & therapeutics · 2026Article
- Isoacteoside alleviates LPS-induced depressive-like behaviors in mice by inhibiting neuroinflammation through regulating microglial polarization and oxidative stress.Behavioral and brain functions : BBF · 2025Article
- Maternal choline supplementation in neurodevelopmental disorders: mechanistic insights from animal models and future directions.Nutritional neuroscience · 2025Review
- Review
- Choline in immunity: a key regulator of immune cell activation and function.Frontiers in immunology · 2025Review
- AIMP1: multifunctional regulator in physiology and pathology with therapeutic implications.PeerJ · 2025Review
- Bibliometric analysis and visualization of lipid droplets in the central nervous system: research hotspots and Frontiers (2000-2024).Frontiers in aging neuroscience · 2025Article
- Irisin Attenuates Neuroinflammation Targeting the NLRP3 Inflammasome.Molecules (Basel, Switzerland) · 2024Article
- Maternal choline supplementation modulates cognition and induces anti-inflammatory signaling in the prefrontal cortices of adolescent rats exposed to maternal immune activation.Brain, behavior, & immunity - health · 2024Article
- Dual-phase SilMA hydrogel: a dynamic scaffold for sequential drug release and enhanced spinal cord repair via neural differentiation and immunomodulation.Frontiers in bioengineering and biotechnology · 2024Article
- Novel Combination of Choline withInternational journal of molecular sciences · 2023Article
- Licochalcone E, a β-Amyloid Aggregation Inhibitor, Regulates Microglial M1/M2 Polarization via Inhibition of CTL1-Mediated Choline Uptake.Biomolecules · 2023Article
- Protective Effects of Choline against Inflammatory Cytokines and Characterization of Transport in Motor Neuron-like Cell Lines (NSC-34).Pharmaceutics · 2022Article
- Unraveling the emerging role of glial heterogeneity in neuropathic pain: from pathological mechanisms to therapeutic Frontiers.Frontiers in neurologyReview
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroglia are key cells of the immune system in the central nervous system and are suggested to be deeply involved in the development of neurodegenerative diseases. It is well known that microglia have functional plasticity, with an inflammatory M1 phenotype and an anti-inflammatory M2 phenotype. Inhibition of choline transport in macrophages has been reported to suppress the secretion of inflammatory cytokines. However, the role of the choline transport system in regulating microglial M1/M2 polarization has not been fully elucidated to date. In this study, we investigated the mechanism of choline uptake in microglia, and its association with microglial M1/M2 polarization.
methodsThe immortalized mouse microglial cell line SIM-A9 was used for [
resultsCholine transporter-like protein (CTL) 1 and CTL2 were highly expressed in SIM-A9 cells, and CTL1 and CTL2 were localized in the plasma membrane and mitochondria, respectively. Functional analysis of choline uptake demonstrated the existence of Na
conclusionsOur results suggest that inhibition of CTL1-mediated choline uptake in microglia preferentially induces M2 microglia polarization, which is a potential therapeutic approach for inflammatory brain diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.